Neural Communication Flashcards
what is a synapse?
where a neuron and postsynaptic cell communicate
what are the components of a synapse?
a presynaptic terminal, postsynaptic membrane, and a synaptic cleft b/w the 2
axodendritic synapse
pre=axon
post=dendrite
most common synapse found in the body
axosomatic synapse
pre=axon
post=soma
axoaxonic synapse
pre and post=axon
axon terminal can synapse on distal axon or extreme distal axon near the terminal
dendrodendritic synapse
pre and post=dendrite
dendrite of one neuron synapsing on the dendrite of another neuron
not very common-only localized in certain areas for the brain
may be bidirectional signaling
may occur in diseased state where axodendritic synapses are damaged
what are the 2 forms of synaptic transmission?
electrical and chemical synapses
electrical synapses
gap junctions enable rapid and synchronized activity of many neurons
pore connections allow AP though pre and post
beneficial in cardiac muscle and its neurons
chemical synapses
key feature: synaptic vesicles filled with NTs
complex=slower but more flexible
- AP reaches presynaptic terminal and vesicles are brought down to terminal membrane
- Ca2+ enters presynaptic terminal through voltage gated Ca2+ channels bc inside has become more positive
- Ca2+ binds to docking proteins (SNARE) and vesicles fuse to membrane
- exocytosis: NT released into cleft
- NT binds to receptors on postsynaptic membrane and opens ion channels (ligand gated)
what are the effects of Botox
snips proteins that make up SNARE complex=no ACh into the cleft=no muscle contraction
no exocytosis of ACh
muscle paralytic
what happens to a NT after it’s used?
NT have to be inactivated/removed from receptors
what are the 3 mechanisms to eliminate NTs?
reuptake, degradation, diffusion
how does reuptake get rid of used NTs?
the NT is taken up, repackaged, and recycled
how does degradation get rid of used NTs?
when a NT is unbound and just existing in the cleft, an enzyme comes and deactivates it
how does diffusion get rid of used NTs?
the NT just diffuses away after it has done its job
what is an excitatory postsynaptic potential?
when the ion channel opens, makes the inside more positive, and depolarizes
how does the sodium channel result in an EPSP?
there is more sodium outside the cell, so when the channel opens, sodium will flow in making the inside more positive causing a depolarization
what is an inhibitory postsynaptic potential?
when the ion channel opens, makes the inside more negative, and depolarizes/hyperpolarizes
inhibits APs
how does the chloride channel result in an IPSP?
there is more chloride outside the cell, so when the channel opens, chloride flows in making the inside more negative causing a depolarization/repolarization
summation of postsynaptic potentials
one excitatory potential=depolarization
2 excitatory potentials=larger depolarization
inhibitory potential=some hyperpolarization
excitatory and inhibitory potential=depolarization if depolarization amplitude is greater than the inhibitory amplitude
2 excitatory and inhibitory potentials=depolarization larger than 1 excitatory and inhibitory but smaller than just 2 excitatory
what is presynaptic facilitation
a neuron excites the presynaptic neuron increasing transmission resulting in a large depolarization (EPSP)
what is presynaptic inhibition?
a neuron inhibits the presynaptic neuron decreasing transmission resulting in a smaller depolarization or hyperpolarization (IPSP)
what is presynaptic facilitory modulation of NT release?
an excitatory neuron increases the amount of NT released from the presynaptic neuron
what is presynaptic inhibitory modulation of NT released?
action of an inhibitory neuron on an axon decreases the amount of NT released from the presynaptic neuron
not every receptor is occupied so the response is decreased
what is a real world example of presynaptic modulation of NT released?
pain perception:
when you think about a cut more it hurts more bc more NT is released
when you think about a cut less, it hurts less bc less NT is released
what are the modulations of receptors?
down regulation and upregulation
what is downregulation?
internalization decreases the number of receptors
inactivation/desensitization decreases the number of active receptors
what is upregulation?
when the number of receptors increase or the receptors become hypersensitive
are upregulation and downregulation reversible?
yes!
what are the 2 types of transmission speeds?
fast transmission and slow transmission
what is another name for fast transmission?
ionotropic
what is another name for slow transmission?
metabotropic
what is fast (ionotropic) transmission?
ligand-gated channels
a NT binds to the receptors, channels open, and ions flow through the channels
what is slow (metabotropic) transmission? what are the 2 types? what do they in
more steps involved makes it slower and more flexible
G-protein coupled receptors:
- a protein is embedded in the membrane
- NT binds to the receptor, conformational changes occur, G-protein is activated, subunits float somewhere else
volume transmission:
- extrasynaptic release
- neuronal communication at variable distances
- NT not released into the cleft
- no particular target tissue
how long does fast (ionotropic) transmission occur?
a millisecond to a minute
how long does slow (metabotropic) transmission occur?
100s of milliseconds to days
cholinergic
ACh
glutamatergic
glutamate
GABAergic
GABA
glycinergic
glycine
(nor)adrenergic
norepinephrine/epinephrine
dopaminergic
dopamine
serotonergic
serotonin
histaminergic
histamine
how are neurons classified?
by the NT they produce, release, or respond to
ACh
excitatory
nicotinic
- ionotropic
- NMJ and CNS
- Alzheimers
muscarinic
- metabotropic
- CNS and PNS
- parasympathetic
glutamate
excitatory
ionotropic
development, learning, and memory formation
non-NMDA
- AMPA and Kainate receptors
- sodium in=depolarization
NMDA:
- glycine acts a agonist
- magnesium block moved by depolarization of non-NMDA, then sodium and calcium can move in and potassium out
GABA
inhibitory
CNS
GABAa
- ionotropic
- ligand-gated Cl- channels open and allow Cl- in making the inside more negative leading to a hyperpolarization
GABAb
- metabotropic
pathology: seizure, involuntary contraction, anxiety (over excitation of the brain)
glycine
Inhibitory
BS and SC
one of the most abundant inhibitory NTs
learning and memory
ligand-gated Cl- channels open allowing Cl- in making the inside more negative causing a hyperpolarization
involved in NMDA receptor activation
pathology: (not enough) involuntary contractions
dopamine
excitatory or inhibitory
motor control, cognition, reward mechanism, motivation
metabotropic
all throughout brain
pathology: addiction, Parkinson’s disease, schizophrenia
norepinephrine (NE)
inhibitory or excitatory
attention and arousal
sympathetic: increased HR, BP, resp rate, vasodilation, vasoconstriction
metabotropic
too much=panic disorder, PTSD
epinephrine closely resembles NE
serotonin
inhibitory
ionotropic and metabotropic
sleep, arousal, cognition, motor function, mood, pain perception
pathology-depression (lack of serotonin)
amines
redundancy
complicates treatment bc it’s hard to know which NT is contributing to symptoms the most
NE, serotonin, and dopamine
opioid peptides
inhibitory
endorphins, enkephalin, dynorphin
inhibit pain perception
SC, hypothalamus, BS
substance P
excitatory
released by injured tissue and stimulates nerve endings at site of injury
CNS:
- relays pain signal from SC to brain
- hypothalamus and cerebral cortex
- pathology-pain syndrome
one of the most common neuropeptides in the body
nociceptive neurons
volume transmission-metabotropic
nitric oxide
excitatory
gasotransmitter
acts through diffusion so it doesn’t require a receptor or membrane
vasodilation
long-term potentiation
seizure disorder
co-transmission
multiple neurons released at the same synapse or from the same neuron
increased stimulus strength
pain info
depolarization=release of glutamate and substance P
slow pain and fast pain
what are NT agonists
bind to receptors and has the same effects of the normal NT
same affinity and effects
what are NT antagonists
bind to receptors and impedes the effects
prevents release of NT
ACE inhibitor, NMDA blocker, Botox
